Although the cardiovascular and respiratory systems closely interact to provide gas transport to and from the tissues, the control of the two systems is generally studied in isolation from each other, and it is not understood how integrated cardiorespiratory responses arise. For example, the mechanisms by which cardiac output and ventilation rise by just the right amount to keep arterial pCO2 constant during exercise is unknown. The long term goal of the work is to clarify the mechanisms by which the cardiovascular and respiratory systems interact to produce integrated response to stimuli. The proposed project will characterize the influence of low and high pressure receptors on respiration, and examine whether these receptors contribute significantly to the ventilatory response to exercise. First, the ventilatory responses to hemodynamic changes in the carotid sinuses will be determined in anesthetized dogs. A perfusion system will be used which allows changing pressure and flow independently. The factors considered will include: possible timing of pressure changes within the respiratory cycle, effects of aortic baroreceptors and vagus on the responses, and the relative roles of baroreceptors and chemoreceptors. Second, the ventilatory responses to hemodynamic changes in the right chambers of the heart will be determined using a pump to keep venous return constnt at any desired level. Third, exercise will be simulated by electrically stimulating the cut hind-limb motor nerves of anesthetized dogs. The hemodynamic component of the exercise response will be disrupted at either the high pressure and low-pressure receptors, and the resulting changes in the ventilatory response examined. We shall test the hypothesis that hemodynamic mechanoreceptors are at least partially responsible for the unexplained isocapnic hyperpnea of exercise.